We primarily wish to study suppressor cell activity with various lymphoreticular neoplasms. This calls for developing and understanding suppressor mechanisms of both cellular and humoral immunity. We have standardized two suppressor mechanisms on T cell proliferation. One (ACSS) is mediated by monocytoid cells and is determined by cell concentration (J. Immunol. 119:173, 1973). The second (ISS) is mediated by T lymphocytes and requires preactivation with concanavalin A. Both suppressor systems have been standardized with normal blood and shown not to decline in vigor at least through the sight age decade. The ACSS, but not the ISS, is effected by a cell that adheres to glass wool. The ISS effector cell loses activity after one day in culture, while the ACSS effector cell remaine active through five days of culture. The ISS effector cell is sensitive to 6500R while the ACSS cell resists 8500R. Neither effector cell is sensitive to hydrocortisone. After considerable difficulty, we have acquired the ability to measure unstimulated and mitogen stimulated immunoglobulin synthesis by cultured leukocytes. Next, we wish to see if immunoglobulin synthesis is regulated by the ACSS and/or ISS and conduct studies on blood and tumor cells from patients with lymphoreticular neoplasms. We have also developed a bioassay for circulating thymic hormone. A forth-coming publication will show that with mycosis fungoides, a T cell neoplasms there is an excess of a T cell inducing substance that is distinct from the hormone thymopoietin in its properties.